Yersinia pseudotuberculosis

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Yersinia pseudotuberculosis
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Yersinia
Species: Y. pseudotuberculosis
Binomial name
Yersinia pseudotuberculosis
(Pfeiffer 1889)
Smith & Thal 1965

Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like(深紅色,緋,緋色の,緋色(の)(ひいろ),ひ色(濃い明かるい赤色)/あかね色,ひ色(濃い明かるい赤色),あかね色,深紅色の) fever in humans, who occasionally(たまに,時折,時々,★"必要に応じて"とか,"何か起きたときに"と考えると理解し易い / You will occasionally be required to tune your system.) get infected(伝染する) zoonotically, most often through the food-borne route.[1] Animals are also infected(伝染する) by Y. pseudotuberculosis. The bacterium is urease positive.

Pathogenesis[edit]

Yersinia pseudotuberculosis
Classification and external resources
Yersinia pestis scanned with electron micrograph.jpg
Yersinia scanned with electron micrograph
ICD-10 A04.8, A28.2
DiseasesDB 14237
eMedicine article/226871
MeSH D015012

In animals, Y. pseudotuberculosis can cause tuberculosis(結核;略:TB)-like symptoms,(徴候,柱,兆候,症状,症候,兆し) including localized(一地方に集まる,地方化する) tissue(ティッシュペーパー,組織) necrosis((No gloss)) and granulomas in the spleen(脾臓(ひぞう)), liver(肝臓,の生活者(a hearty liverなど),レバー,きも,茶褐色), and lymph(リンパ,リンパ液,血清,痘苗) nodes(節点,【ネットワーク】ノード).

In humans, symptoms(徴候,柱,兆候,症状,症候,兆し) of Far East scarlet-like(深紅色,緋,緋色の,緋色(の)(ひいろ),ひ色(濃い明かるい赤色)/あかね色,ひ色(濃い明かるい赤色),あかね色,深紅色の) fever are similar to those of infection(伝染病,伝染,感染,感化,影響) with Yersinia enterocolitica (fever and right-sided abdominal(腹部) pain), except that the diarrheal component(構成している,成文,成分,構成要素) is often absent, which sometimes makes the resulting condition difficult to diagnose.(診断する) Y. pseudotuberculosis infections(伝染病,伝染,感染,感化,影響) can mimic((mimicked,mimicking) 1.〜をまねる,まねてからかう,よく似る,2.にせの,模倣の,模造の,3.模倣者,模倣者,にせの,人まねをする動物,物まねする,まねの) appendicitis(【病名】虫垂炎(いわゆる盲腸炎)), especially in children and younger adults, and, in rare cases, the disease may cause skin complaints (erythema nodosum), joint stiffness and pain (reactive((刺激に対して)敏感な,反応の早い,反作用的な) arthritis(関節炎)), or spread of bacteria(バクテリア) to the blood (bacteremia).

Far East scarlet-like(深紅色,緋,緋色の,緋色(の)(ひいろ),ひ色(濃い明かるい赤色)/あかね色,ひ色(濃い明かるい赤色),あかね色,深紅色の) fever usually becomes apparent((目に)明らかな,はっきりと理解できる,明白な,見かけの,外見上の) five to 10 days after exposure(暴露,さらすこと,露出,さらす,露光,照射,公開,発覚,爆射,凍傷,露見) and typically lasts one to three weeks without treatment.(1.取り扱い,扱い,治療,待遇,処理,処置,2.台本,シナリオ) In complex cases or those involving(人を巻き込む,巻き込む,を含む,必要とする,意味する) immunocompromised patients, antibiotics(抗生物質) may be necessary for resolution;(1.決議案,決議,決定,裁決,2.決心,決意,決断,果断,解決,3.転換,変換,4.分解,分解能解像度) ampicillin, aminoglycosides, tetracycline, chloramphenicol, or a cephalosporin may all be effective.

The recently described syndrome(シンドローム,【医学】症候群(病的諸傾向),一連の事物(事件),ある状況下での行動様式) "Izumi-fever" has been linked(連結するもの,連接棒,を連結する,を握る,組み合う,たいまつ,輪,きずな,連鎖,可溶接解片,つながり,鎖の環,つながる,つなぐ) to infection(伝染病,伝染,感染,感化,影響) with Y. pseudotuberculosis.[2]

The symptoms(徴候,柱,兆候,症状,症候,兆し) of fever and abdominal(腹部) pain mimicking((mimicked,mimicking) 1.〜をまねる,まねてからかう,よく似る,2.にせの,模倣の,模造の,3.模倣者,模倣者,にせの,人まねをする動物,物まねする,まねの) appendicitis(【病名】虫垂炎(いわゆる盲腸炎)) (actually from mesenteric lymphadenitis) [3][4][5] associated(1.社員,仲間,準会員,coworker, colleague,2.結びつける,関連づける,連想する,結合させる,交際する,思い出す,仲間に加える,連合させる) with Y. pseudotuberculosis infection(伝染病,伝染,感染,感化,影響) are not typical of the diarrhea(【病名】下痢) and vomiting(嘔吐する,激しく流出する,へどを吐く,もどす,吐く) from classical(古典文学の,古典の,古典的な,古典主義の,最高級の,一流の,クラシックの,一般教養的な,古典派の) food poisoning incidents.(1.起こりやすい,ありがちな,2.出来事,事件,紛争,事変(ささいに見えるが大きな外交問題に発展するような) / What hit Tokyo was not just another incident of urban terrorism. - Asiaweek) Although Y. pseudotuberculosis is usually only able to colonize(植民する) hosts by peripheral(周辺の,末梢性の) routes and cause serious disease in immunocompromised individuals, if this bacterium gains access(にアクセスする,交通の便,接近,近づき,発作,面接,アクセス,手引き) to the blood stream, it has an LD50 comparable(比較できるほどの,比較できる,匹敵する,同程度の) to Y. pestis at only 10 CFU.[6]

Relationship to Y. pestis[edit]

Genetically, the pathogen((No gloss)) causing plague(1.ペスト,疫病,大発生,2.悩ます,苦しめる), Y. pestis, is very similar to Y. pseudotuberculosis. The plague(1.ペスト,疫病,大発生,2.悩ます,苦しめる) appears to have evolved(発展する/させる,進化する/させる,導きだす,展開する) from Y. pseudotuberculosis about 1500 to 20,000 years ago.[7]

Virulence factors[edit]

To facilitate(容易にする,促進する,楽にする) attachment,(取付け,付着,接着,吸着,付着物,付属物,付属部品,張り付けること,愛情を持つこと,アタッチメント,愛着) invasion,(侵入,殺到,侵害) and colonization((No gloss)) of its host, this bacterium possesses many virulence factors(仲買人,因子,要因,要素,原因,因数). Superantigens, bacterial((No gloss)) adhesions, and the actions of Yops (which are bacterial((No gloss)) proteins(タンパク質,蛋白質,たん白質) once thought to be "Yersinia outer(外の,外側の,客観的な,圏外) membrane(薄膜,膜,皮膜,膜組織) proteins")(タンパク質,蛋白質,たん白質) that are encoded(符合化する) on the "[plasmid] for Yersinia virulence"commonly(一般に,通例,下品に,粗野に,通俗に,普通) known as the pYVcause host pathogenesis and allow the bacteria(バクテリア) to live parasitically.

pYV[edit]

The 70-kb pYV is critical(1.評論[批評]の,2.危機の,重大な,決定的(に重要)な,3.危険な,危ない,危篤の,臨界の) to Yersinia's pathogenicity, since it contains many genes(遺伝子) known to encode(符合化する) virulence factors(仲買人,因子,要因,要素,原因,因数) and its loss gives avirulence of all Yersinia species.(人類,種,種類)[6] A 26-kb "core region"(領域,地域,地帯,地方,分野,範囲,界) in the pYV contains the ysc genes,(遺伝子) which regulate(規則正しくする,を規定する,を制限する,を調節する,調整する,調節する) the expression and secretion(分泌(物,液),隠匿,分泌物) of Yops.[5] Many Ysc proteins(タンパク質,蛋白質,たん白質) also amalgamate((会社など)を合併する) to form a type-III secretory apparatus,(ある目的に必要な器具一式のこと,実験用の装置・器具など,装置,器具) which secretes(〜を隠匿する,を分泌する,隠匿する) many Yops into the host cell cytoplasm((No gloss)) with the assistance of the "translocation apparatus",(ある目的に必要な器具一式のこと,実験用の装置・器具など,装置,器具) constructed of YopB and YopD.[8][9] The core(1.中心,核心,コア,2.芯を取る[抜く],3.中心[中核]的な) region(領域,地域,地帯,地方,分野,範囲,界) also includes yopN, yopB, yopD, tyeA, lcrG, and lcrV, which also regulate(規則正しくする,を規定する,を制限する,を調節する,調整する,調節する) Yops gene(遺伝子) expression and help to translocate secretory Yops to the target cell.[5] For example, YopN and TyeA are positioned as a plug(差し込み,消火栓,栓,プラグ,ソケット,点火栓,をふさぐ,宣伝(する),くり返し宣伝する) on the apparatus(ある目的に必要な器具一式のこと,実験用の装置・器具など,装置,器具) so only their conformational change, induced(生じさせる,勧誘する,人に勧めて〜させる,を引き起こす,させる,強制分娩させる,誘発する) by their interaction(相互作用) with certain host cell membrane(薄膜,膜,皮膜,膜組織) proteins,(タンパク質,蛋白質,たん白質) will cause the unblocking of the secretory pathway.(小道,通路)[5][10] Secretion is regulated(規則正しくする,を規定する,を制限する,を調節する,調整する,調節する) in this fashion so that proteins(タンパク質,蛋白質,たん白質) are not expelled(害虫を駆除する,を追い出す,を追放する,を放出する,発射する,駆逐する,追い出す) into the extracellular matrix(母体,行列,鋳型) and elicit((情報・返答などを)引き出す,導き出す / The command uses the protocol's echo request datagram to elicit an echo response from the specified host.) an immune(免疫の,免疫がある) response. Since this pathway(小道,通路) gives secretion(分泌(物,液),隠匿,分泌物) selectivity, it is a virulence factor.(仲買人,因子,要因,要素,原因,因数)

Effector Yops[edit]

In contrast(正反対のもの,対照,対照させる,相違,対照的に異なる物,引き立つ,対比する) to the ysc and yop genes(遺伝子) listed above, the Yops that act directly on host cells to cause cytopathologic effects – "effector Yops" – are encoded(符合化する) by pYV genes(遺伝子) external(1.外部にある,外の,外部の,外的な,外側の,外用の,形式的な,国外の,表面的な,2.外部,外見,外面) to this core(1.中心,核心,コア,2.芯を取る[抜く],3.中心[中核]的な) region.(領域,地域,地帯,地方,分野,範囲,界)[5] The sole(1.たった一つの,唯一の,一人だけに属する,独占的な,独身の,蹄鉄,2.足の裏,たった一つの,靴底,足の裏,舌平目,底をつける,単独の) exception is LcrV, which is also known as the "versatile Yop" for its two roles as an effector Yop and as a regulatory Yop.[5] The combined(結合する,企業合同,連合する,連合体,結集する) function of these effector Yops permits the bacteria(バクテリア) to resist internalization by immune(免疫の,免疫がある) and intestinal cells and to evade(巧みに逃げる(escape),〜をうまく切り抜ける,(質問などを)はぐらかす,法律の目をくぐる,遂行を怠る,〜を巧みに避ける,避ける) the bactericidal actions of neutrophils and macrophages. Inside the bacterium, these Yops are bound by pYV-encoded Sycs (specific Yop chaperones), which prevent premature(早すぎる,早まった,時期尚早の,尚早の,早計の,盛り上がりの前の) interaction(相互作用) with other proteins(タンパク質,蛋白質,たん白質) and guide the Yops to a type-III secretory apparatus.(ある目的に必要な器具一式のこと,実験用の装置・器具など,装置,器具)[9] In addition to the Syc-Yop complex, Yops are also tagged(に下げ札をつける,決まり文句,札,下げ札,荷札,金具,尾,巻き毛,【車】《米》ナンバープレート) for type III secretion(分泌(物,液),隠匿,分泌物) either by the first 60nt in their corresponding(一致する,対応する,調和する,該当する) mRNA transcript(写し,複写,転写物,謄本) or by their corresponding(一致する,対応する,調和する,該当する) first 20 N-terminal amino acids(1.酸っぱい,2.辛辣な,3.酸,4.《俗語》麻薬,LSD).[4] LcrV, YopQ, YopE, YopT, YopH, YpkA, YopJ, YopM, and YadA are all secreted(〜を隠匿する,を分泌する,隠匿する) by the type-III secretory pathway.(小道,通路)[4][5][10] LcrV inhibits(することを禁ずる,を抑制する,妨げる,抑える) neutrophil((No gloss)) chemotaxis and cytokine production, allowing Y. pseudotuberculosis to form large colonies without inducing(生じさせる,勧誘する,人に勧めて〜させる,を引き起こす,させる,強制分娩させる,誘発する) systemic failure[10] and, with YopQ, contributes(貢献する,寄与する,寄稿する,寄付する) to the translocation process by bringing YopB and YopD to the eukaryotic cell membrane(薄膜,膜,皮膜,膜組織) for pore-formation.(熟考する,考え込む)[4][11] By causing actin filament depolymerisation, YopE, YopT, and YpkA resist endocytosis by intestinal cells and phagocytosis while giving cytotoxic((No gloss)) changes in the host cell. YopT targets Rho GTPase, commonly(一般に,通例,下品に,粗野に,通俗に,普通) named "RhoA", and uncouples it from the membrane,(薄膜,膜,皮膜,膜組織) leaving it in an inactive(活動しない,怠惰な,緩慢な,受身的な,不活発な) RhoA-GDI (guanine nucleotide((No gloss)) dissociation((No gloss)) inhibitor)-bound((No gloss)) state[12] whereas(1.ところが,〜であるのに,一方,2.〜なるが故に,★=while, on the contrary) YopE and YpkA convert(変換させる,転換する,変換する,変える,を改装する,を改心させる,を転用する,変化させる,変化する,転向者,換算される,転向する) Rho proteins(タンパク質,蛋白質,たん白質) to their inactive(活動しない,怠惰な,緩慢な,受身的な,不活発な) GDP-bound states by expressing GTPase activity.[10] YpkA also catalyses serine((No gloss)) autophosporylation, so it may have regulatory functions in Yersinia[13] or undermine(密かに傷つける,の下を掘る,土台を崩す) host cell immune(免疫の,免疫がある) response signal cascades(小滝,滝,滝のように落下する,段々滝(となって落ちる),滝のように落ちる,波状レース飾り,(菊の)懸崖(けんがい)づくり,(電気)縦つなぎ) since YpkA is targeted to the cytoplasmic side of the host cell membrane.(薄膜,膜,皮膜,膜組織)[14] YopH acts on host focal(焦点の(にある)) adhesion(粘着) sites(用地,場所,遺跡,現場,跡,用地を定める) by dephosphorylating several phosphotyrosine residues(残余,残留物,かす,留数,剰余,残基) on focal(焦点の(にある)) adhesion(粘着) kinase (FAK) and the focal(焦点の(にある)) adhesion(粘着) proteins(タンパク質,蛋白質,たん白質) paxillin and p130.[15] Since FAK phosphorylation is involved(人を巻き込む,巻き込む,を含む,必要とする,意味する) in uptake(摂取) of yersiniae[16] as well as T cell and B cell responses to antigen-binding,((No gloss))[10] YopH elicits((情報・返答などを)引き出す,導き出す / The command uses the protocol's echo request datagram to elicit an echo response from the specified host.) antiphagocytic and other anti-immune((No gloss)) effects. YopJ, which shares an operon with YpkA, "...interferes with the mitogen-activated protein(タンパク質,蛋白質,たん白質) (MAP) kinase activities of c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase",[17] leading to macrophage apoptosis.[4] In addition, YopJ inhibits(することを禁ずる,を抑制する,妨げる,抑える) TNF-α release from many cell types, possibly through an inhibitory(抑制する) action on NF-κB, suppressing(抑圧する,鎮定する,抑える,鎮圧する,我慢する,隠す) inflammation(燃焼,炎症) and the immune(免疫の,免疫がある) response.[18] By secretion(分泌(物,液),隠匿,分泌物) through a type III pathway(小道,通路) and localization(局所化) in the nucleus(細胞核,核,原子核,心,中軸) by a vesicle-associated, microtubule-dependent method, YopM may alter host cell growth by binding(1.製本,装丁,2.<契約などが>拘束力のある,表紙,拘束力がある) to RSK (ribosomal S6 kinase), which regulates(規則正しくする,を規定する,を制限する,を調節する,調整する,調節する) cell cycle regulation genes.(遺伝子)[10] Interestingly, YadA has lost its adhesion,(粘着)[19] opsonisation-resisting, phagocytosis-resisting, and respiratory(呼吸の) burst-resisting functions[20][21] in Y. pseudotuberculosis due to a frameshift mutation(変化,突然変異) by a single base-pair deletion((No gloss)) in yadA in comparison(比較,対照,比較対照,比較変化) to yadA in Y. enterocolitica, yet it still is secreted(〜を隠匿する,を分泌する,隠匿する) by type III secretion.(分泌(物,液),隠匿,分泌物)[22] The yop genes,(遺伝子) yadA, ylpA, and the virC operon are considered the "Yop regulon" since they are coregulated by pYV-encoded VirF. virF is in turn thermoregulated. At 37 degrees Celsius, chromosomally encoded(符合化する) Ymo, which regulates(規則正しくする,を規定する,を制限する,を調節する,調整する,調節する) DNA supercoiling around the virF gene,(遺伝子) changes conformation,((No gloss)) allowing for VirF expression, which then up-regulates the Yop regulon.[23]

Adhesion[edit]

Y. pseudotuberculosis adheres(執着する,堅く守る,粘着する,固守する,忠実である,付く) strongly(頑丈に,強く,丈夫に,強硬に,熱心に) to intestinal cells via(〜を経て,経由して,〜によって) chromosomally encoded(符合化する) proteins(タンパク質,蛋白質,たん白質)[4] so that Yop secretion(分泌(物,液),隠匿,分泌物) may occur, to avoid being removed by peristalsis, and to invade target host cells. A transmembrane protein,(タンパク質,蛋白質,たん白質) Invasin, facilitates(容易にする,促進する,楽にする) these functions by binding(1.製本,装丁,2.<契約などが>拘束力のある,表紙,拘束力がある) to host cell αβ1 integrins.[24] Through this binding,(1.製本,装丁,2.<契約などが>拘束力のある,表紙,拘束力がある) the integrins cluster,(1.かたまり,束,一団,群集,(花,果実の)房,群れ,2.群がる,房になる,群生する,集める) thereby(それによって,その結果) activating(放射能を与える,活性化する,活動的にする,活動させる) FAK, and causing a corresponding(一致する,対応する,調和する,該当する) reorganization(1.再編成,改組,改編,2.【金融】再建,立て直し,再編成) of the cytoskeleton.[4][24] Subsequent internalization of bound bacteria(バクテリア) occurs when the actin-depolymerising Yops are not being expressed.[10] The protein(タンパク質,蛋白質,たん白質) encoded(符合化する) on the "attachment invasion(侵入,殺到,侵害) locus"((No gloss)) named Ail also bestows(1.授ける,贈る,与える,2.利用する,<時間・エネルギーなどを>(〜に)費やす) attachment(取付け,付着,接着,吸着,付着物,付属物,付属部品,張り付けること,愛情を持つこと,アタッチメント,愛着) and invasive(侵略的な) abilities upon Yersiniae[25] while interfering with the binding(1.製本,装丁,2.<契約などが>拘束力のある,表紙,拘束力がある) of complement(補足,補部,全数量,補足物,補集合,【文法】補語,補文,補数,乗組員定員,全数,定数,補って完全にする) on the bacterial((No gloss)) surface.[26] To increase binding(1.製本,装丁,2.<契約などが>拘束力のある,表紙,拘束力がある) specificity, the fibrillar pH6 antigen((No gloss)) targets bacteria(バクテリア) to target intestinal cells only when thermoinduced.[27]

Superantigens[edit]

Certain strains(1.〜を緊張させる,をぴんと張る,を痛める,2.種族,血統,気質,素質,傾向,話し[書き]ぶり,旋律,文体,種族,調べ,筋違い,緊張,張る力,負担,張り詰める,努める) of Yersinia pseudotuberculosis express a superantigenic exotoxin, YPM, or the Y. pseudotuberculosis-derived mitogen, from the chromosomal ypm gene.(遺伝子)[28] YPM specifically(明確に,特に,とりわけ,具体的に,具体的には,特別に) binds and causes the proliferation(増殖,急増) of T lymphocytes expressing the Vβ3, Vβ7, Vβ8, Vβ9, Vβ13.1, and Vβ13.2 variable(変わりやすい,気まぐれな,可変の,変化するもの,一定しない,不定の,変えられる) regions(領域,地域,地帯,地方,分野,範囲,界) [29] with CD4+ T cell preference,(好み,(好みによる)選択,選り好み,ひいき,好物,優先権,先取権,優先,(他よりも)好むこと,嗜好) although activation(現役編入) of some CD8+ T cells occurs.[3] This T cell expansion(膨張,発展,展開(式),拡張) can cause splenomegaly coupled with IL-2 and IL-4 overproduction.[30] Since administering(施行する,管理する,与える) anti-((No gloss))TNF-α and anti-((No gloss))IFN-γ monoclonal antibodies(免疫体,抗体) neutralizes(中立化する,中和する) YPM toxicity in vivo,[28] these cytokines are largely responsible for the damage caused indirectly by the exotoxin. Strains that carry the exotoxin gene(遺伝子) are rare in Western countries, where the disease, when at all apparent,((目に)明らかな,はっきりと理解できる,明白な,見かけの,外見上の) manifests(1.明白な,明らかな,2.乗客名簿,積み荷録,3.明らかにする,証明する) itself largely with minor symptoms,(徴候,柱,兆候,症状,症候,兆し) whereas(1.ところが,〜であるのに,一方,2.〜なるが故に,★=while, on the contrary) more than 95% of strains(1.〜を緊張させる,をぴんと張る,を痛める,2.種族,血統,気質,素質,傾向,話し[書き]ぶり,旋律,文体,種族,調べ,筋違い,緊張,張る力,負担,張り詰める,努める) from Far Eastern countries contain ypm[31] and are correlated(相互に関連がある,相互関係を持たせる) with Izumi fever and Kawasaki disease.[32] Although the superantigen poses the greatest threat to host health, all virulence factors(仲買人,因子,要因,要素,原因,因数) contribute(貢献する,寄与する,寄稿する,寄付する) to Y. pseudotuberculosis viability in vivo and define(本質を明らかにする,を定義する,範囲を限定する,定義する) the bacterium’s pathogenic((No gloss)) characteristics. Y. pseudotuberculosis can live extracellularly due to its formidable(なまなかでない,圧迫感がある,手ごわい) mechanisms(機構,機械装置,仕組み,手段,メカニズム) of phagocytosis and opsonisation resistance(1.電気抵抗,2.抵抗,反抗,抗争,反対,妨害,敵対,抵抗力,電気抵抗,抵抗,レジスタンス) through the expression of Yops and the type III pathway;(小道,通路)[9] yet, by limited pYV action, it can populate(に人を居住させる,住む) host cells, especially macrophages, intracellularly to further evade(巧みに逃げる(escape),〜をうまく切り抜ける,(質問などを)はぐらかす,法律の目をくぐる,遂行を怠る,〜を巧みに避ける,避ける) immune(免疫の,免疫がある) responses and be disseminated((種子など)をまく,(意見など)を広める,ばらまく,広める,散布する,広まる) throughout the body.[33]

YpM
PDB 1pm4 EBI.jpg
crystal structure of yersinia pseudotuberculosis-derived mitogen (ypm)
Identifiers
Symbol YpM
Pfam PF09144
InterPro IPR015227
SCOP 1pm4
SUPERFAMILY 1pm4

Yersinia pseudotuberculosis is a Gram-negative food-borne pathogen((No gloss)) that causes gastroenteritis(胃腸炎).

Function[edit]

Yersinia pseudotuberculosis-derived mitogens (YpM) are superantigens, which are able to excessively(過度に) activate(放射能を与える,活性化する,活動的にする,活動させる) T cells by binding(1.製本,装丁,2.<契約などが>拘束力のある,表紙,拘束力がある) to the T cell receptor((No gloss)). Since YpM can activate(放射能を与える,活性化する,活動的にする,活動させる) large numbers of the T cell population, this leads the release of inflammatory(扇動的な,怒りをかきたてる,感情を刺激する,激昂させる,煽動的な) cytokines.

Structure[edit]

Members of this family of Yersinia pseudotuberculosis mitogens adopt a sandwich structure consisting of 9 strands(座礁する(させる),岸に上がる,立ち往生する,取り残す(される),困る(らせる),2.岸,岸辺より糸,房,岸,糸,座礁させる) in two beta((No gloss)) sheets, in a jelly-roll topology. YpM molecular(分子の) weight is about 14 kDa. Structurally, it is unlike(似ていない,異なっている) any other superantigen, but is remarkably similar to the tumour((No gloss)) necrosis((No gloss)) factor(仲買人,因子,要因,要素,原因,因数) and viral(ウイルスの,ウイルスによっておこる) capsid proteins.(タンパク質,蛋白質,たん白質) This suggests a possible evolutionary(進化した) relationship.[34]

Subfamilies[edit]

Some highly homologous((No gloss)) variants(1.異なった,相違する,一致しない,種々の,変種の,2.変形,変化) of YPM have been characterized,(の特性を示す,特徴づける) including YPMa, YPMb, and YPMc.

References[edit]

  1. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  2. ^ Jani, Asim (2003). "Pseudotuberculosis (Yersina)". Retrieved 2006-03-04. 
  3. ^ a b Carnoy, C., N. Lemaitre, and M. Simonet. 2006. The superantigenic toxin of Yersinia pseudotuberculosis, p.862-871. In J. E. Alouf and M. R. Popoff (ed.), The comprehensive sourcebook of bacterial protein toxins, 3rd ed. Elsevier Ltd., Burlington, MA.
  4. ^ a b c d e f g Robins-Browne, R. and E. Hartland. 2003. Yersinia species, p.323-355. In M. D. Miliotis and J. W. Bier (ed.), International handbook of foodborne pathogens. Marcel Dekker, Inc., New York, NY.
  5. ^ a b c d e f g Lindler, L. 2004. Virulence plasmids of Yersinia: characteristics and comparison, p.423-437. In B. E. Funnel and G. J. Phillips (ed.), Plasmid biology. ASM Press, Washington, DC.
  6. ^ a b Brubaker, R. 1983. The Vwa+ virulence factor of yersiniae: the molecular basis of the attendant nutritional requirement for Ca++. Rev. Infect. Dis. 5:S748-S758.
  7. ^ Achtman, M.; Zurth, K., Morelli, G., Torrea, G., Guiyoule, A., & Carniel; E. (23 November 1999). "Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis". Proceedings of the National Academy of Sciences 96 (24): 14043–14048. doi:10.1073/pnas.96.24.14043. PMC 24187. PMID 10570195. Retrieved 21 March 2013. 
  8. ^ Iriarte, M. and G. Cornelis. 1999. Identification of SycN, YscX, and TscY, three new elements of the Yersinia yop virulon. J. Bacteriol. 181:675-680.
  9. ^ a b c Cornelis, G., A. Boland, A. Boyd, C. Geuijen, M. Iriarte, C. Neyt, M.-P. Sory, and I. Stainer. 1998. The virulence of Yersinia, an antihost genome. Microbiol. Mol. Biol. Rev. 62:1315-1352.
  10. ^ a b c d e f g Lee, V., C. Tam, and O. Schneewind. 2000. LcrV, a substrate for Yersinia enterocolitica type III secretion, is required for toxin targeting into the cytosol of HeLa cells. J. Biol. Chem. 275:36869-36875.
  11. ^ Zumbihl, R., M. Aeptelbacher, A. Andor, C. Jacobi, K. Ruckdeschel, B. Rouot, and J. Heesemann. 1999. The cytotoxin YopT of Yersinia enterocolitica induces modification and cellular redistribution of the small GTP-binding protein RhoA. J. Biol. Chem. 274:29289-29293.
  12. ^ Persson, C., N. Carballeira, H. Wolf-Watz, M. Fallman. 1997. The PTPase YopH inhibits uptake of Yersinia, tyrosine phosphorylation of p130Cas and FAK, and the associated accumulation of these proteins in peripheral focal adhesions. EMBO J. 16:2307-2318.
  13. ^ Haokansson, S., E. Galyov, R. Rosqvist, H. Wolf-Watz. 1996. The Yersinia YpkA Ser/Thr kinase is translocated and subsequently targeted to the inner surface of the HeLa plasma membrane. Mol. Microbiol. 20:593-603.
  14. ^ Ruckdeshel, K., J. Machold, A. Roggenkamp, S. Schubert, J. Pierre, R. Zumbihl, J. Liautard, J. Heesemann, and B. Rouot. 1997. Yersinia eneterocolitica promotes deactivation of macrophage mitogen-activated protein kinases extracellular signal-related kinase-1/2, p38, and c-Jun NH2-terminal kinase. Correlation with its inhibitory effect on tumor necrosis factor-α production. J. Biol. Chem. 272:15920-15927.
  15. ^ Alrutz, M. and R. Isberg. 1998. Involvement of focal adhesion kinase in invasion-mediated uptake. Proc. Natl. Acad. Sci. 95:13658-13663.
  16. ^ Galyov, E., S. Hakansson, A. Forsberg, and H. Wolf-Watz. 1993. A secreted protein kinase of Yersinia pseudotuberculosis is an indispensable virulence determinant. Nature 361:730-732.
  17. ^ Boland, A. and G. Cornelis. 1998. Role of YopP in suppression of tumor necrosis factor alpha release by macrophages during Yersinia infection. Infect. Immun. 66:1878-1884.
  18. ^ Skurnik, M., Y. el Tahir, M. Saarinen, S. Jalkanen, and P. Toivanen. 1994. YadA mediates specific binding of enteropathogenic Yersinia enterocolitica to human intestinal submucosa. Infect. Immun. 62:1252-1261.
  19. ^ China, B., M. Sory, B. N’Guyen, M. de Bruyere, and G. Cornelis. 1993. Role of the YadA protein in prevention of opsonisation of Yersinia enterocolitica by C3b molecules. Infect. Immun. 61:3129-3136.
  20. ^ China, B., B. N’Guyen, M. de Bruyere, and G. Cornelis. 1994. Role of YadA in resistance of Yersinia enterocolitica to phagocytosis by human polymorphonuclear leukocytes. Infect. Immun. 62:1275-1281.
  21. ^ Han, Y. and V. Miller. 1997. Reevaluation of the virulence phenotype of the inv yadA double mutants of Yersinia pseudotuberculosis. Infect. Immun. 65:327-330.
  22. ^ Cornelis, G., C. Sluiters, I. Delor, D. Geib, K. Kaniga, C. Lambert de Rouvroit, M.-P. Sory, J.-C. Vanooteghem, and T. Michiels. 1991. ymoA, a Yersinia enterocolitica chromosomal gene modulating the expression of virulence functions. Mol Microbiol. 5:1023-1034.
  23. ^ Isberg, R. and G. Van Nhieu. 1994. Two mammalian cell internalization strategies used by pathogenic bacteria. Annu. Rev. Genet. 28:395-422.
  24. ^ a b Miller, V. 1992. Yersinia invasion genes and their products. ASM News 58:26-33.
  25. ^ Bliska, J. and S. Falkow. 1992. Bacterial resistance to complement killing mediated by the Ail protein of Yersinia enterocolitica. Proc. Natl. Acad. Sci. 89:3561-3565.
  26. ^ Lindler, L. and B. Tall. 1993. Yersinia pestis pH 6 antigen forms fimbriae and is induced by intracellular association with macrophages. Mol. Microbiol. 8:311-324.
  27. ^ Miyoshi-Akiyama, T., W. Fujimaki, X. Yan, J. Yagi, K. Imanishi, H. Kato, K. Tomonari, and T. Uchiyama. 1997. Identification of murine T cells reactive with the bacterial superantigen Yersinia pseudotuberculosis-derived mitogen (YPM) and factors involved in YPM-induced toxicity in mice. Microbiol. Immunol. 41:345-352.
  28. ^ a b Uchiyama, T., T. Miyoshi-Akiyama, H. Kato, W. Fujimaki, K. Imanishi, and X. Yan. 1993. Superantigenic properties of a novel mitogenic substance produced by Yersinia pseudotuberculosis isolated from patients manifesting acute and systemic symptoms. J. Immunol. 151:4407-4413.
  29. ^ Carnoy, C., C. Loiez, C. Faveeuw, C. Grangette, P. Desreumaux, and M. Simonet. 2003. Impact of the Yersinia pseudotuberculosis-derived mitogen (YPM) on the murine immune system. Adv. Exp. Med. Biol. 529:133-135.
  30. ^ Yoshino, K., T. Ramamurthy, G. Nair, H. Fukushima, Y. Ohtomo, N. Takeda, S. Kaneko, and T. Takeda. 1995. Geographical heterogeneity between Far East and Europe in prevalence of ypm gene encoding the novel superantigen among Yersinia pseudotuberculosis strains. J. Clin. Microbiol. 33:3356-3358.
  31. ^ Fukushima, H., Y. Matsuda, R. Seki, M. Tsubokura, N. Takeda, F. Shubin, I. Paik, and X. Zheng. 2001. Geographical heterogeneity between Far Eastern and Western countries in prevalence of the virulence plasmid, the superantigen Yersinia pseudotuberculosis-derived mitogen, and the high-pathogenicity island among Yersinia pseudotuberculosis strains. J. Clin. Microbiol. 39:3541-3547.
  32. ^ Nikolova, S., H. Najdenski, D. Wesselinova, A. Vesselinova, D. Kazatchca, and P. Neikov. 1997. Immunological and electronmicroscopic studies in pigs infected with Yersinia enterocolitica O:3. Zentralbl. Bakteriol. 286:503-510.
  33. ^ Smith, M. 1992. Destruction of bacteria on fresh meat by hot water. Epidemiol. Infect. 109:491-496.
  34. ^ Donadini R, Liew CW, Kwan AH, Mackay JP, Fields BA (January 2004). "Crystal and solution structures of a superantigen from Yersinia pseudotuberculosis reveal a jelly-roll fold". Structure 12 (1): 145–56. doi:10.1016/j.str.2003.12.002. PMID 14725774. 

This article(論文,論説,記事,品物,一品,契約,条項,【文法】冠詞) incorporates(1.具体化する,法人組織にする,入れる,合併する,加入させる,組込む,受け入れる,組み入れる,2.法人組織の) text from the public domain(領地,領土,範囲,変域,統治地域,領域,分野,所有地) Pfam and InterPro IPR015227

External links[edit]